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Transient cerebral ischemia was induced by 15 min of bilateral common carotid artery occlusion (BCCAO) 24 h after A\u03b2 injection.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Results<\/jats:title>\n                <jats:p>A\u03b2 injection in WT induced a cognitive decline, whereas BCCAO did not cause a significant cognitive deficit. In contrast, WT with BCCAO following A\u03b2 injection exhibited more marked cognitive decline compared to A\u03b2 injection alone, in concert with increases in superoxide anion production, nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity, and expression of p22phox, p40phox, monocyte chemoattractant protein (MCP)-1 and interleukin (IL)-1\u03b2 in the hippocampus, and upregulation of RAGE (receptor for advanced glycation end product), an A\u03b2 transporter. BCCAO following A\u03b2 injection further enhanced neuronal pyknosis in the hippocampus, compared with BCCAO or A\u03b2 injection alone. In contrast, smAT<jats:sub>2<\/jats:sub> did not show a cognitive decline, increase in oxidative stress, inflammation, and RAGE level or neuronal pyknosis, which were induced by BCCAO with\/without A\u03b2 injection in WT.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Conclusions<\/jats:title>\n                <jats:p>Transient cerebral ischemia might worsen A\u03b2 infusion-mediated cognitive decline and vice versa, with possible involvement of amplified oxidative stress and inflammation and impairment of the RAGE-mediated A\u03b2 clearance system, contributing to exaggerated neuronal degeneration. AT<jats:sub>2<\/jats:sub> receptor activation in VSMC could play an inhibitory role in this cognitive deficit.<\/jats:p>\n              <\/jats:sec>","DOI":"10.1186\/s12974-020-01775-8","type":"journal-article","created":{"date-parts":[[2020,4,7]],"date-time":"2020-04-07T13:02:58Z","timestamp":1586264578000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":14,"title":["Deterioration of cognitive function after transient cerebral ischemia with amyloid-\u03b2 infusion\u2014possible amelioration of cognitive function by AT2 receptor activation"],"prefix":"10.1186","volume":"17","author":[{"given":"Li-Juan","family":"Min","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jun","family":"Iwanami","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Masachika","family":"Shudou","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hui-Yu","family":"Bai","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bao-Shuai","family":"Shan","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Akinori","family":"Higaki","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Masaki","family":"Mogi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Masatsugu","family":"Horiuchi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2020,4,7]]},"reference":[{"key":"1775_CR1","doi-asserted-by":"publisher","first-page":"98","DOI":"10.1016\/j.jalz.2010.01.010","volume":"6","author":"A Wimo","year":"2010","unstructured":"Wimo A, Winblad B, Jonsson L. 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